Iron and Inflammation

It has been well documented that the anaemia of chronic disease, ACD, results in a lowering of various haematological parameters. Several mediators are involved, among them histamine, serotonin, bradykinin, prostaglandins and, as found more recently, cytokines and nitric oxide. ACD is a parameter of systemic autoimmune disorders. The severe inflammatory stimuli lead to several systemic changes, mediated by inflammation-associated cytokines, e.g. IL-6, IL-1 TNFa, TGF beta that regulate hepatic synthesis of the acute phase proteins.

In rheumatoid arthritis iron accumulates in the joints, specifically the synovium, and this was reputed to exacerbate joint injury by the production of ROS. Later studies indicated that ischaemia/reperfusion injury, associated with increased iron loading, might be more relevant to the joint damage. Circulating levels of TNFa and IL-1b serum levels are significantly increased in RA with ACD. RA patients treated with TNFa antibodies show disease improvement including an increase in haemoglobin levels. The most controversial and stimulating aspect of the pathogenesis of ACD in system autoimmune disease is the role of iron metabolism and nitric oxide; the latter, as we have already mentioned, contributes to the regulation of iron metabolism. Both iron deficiency and iron overload influence the proliferation of B and T lymphocytes and differentially affect T-helper and TH-2 lymphocytes. Furthermore TH-1 cytokines and TH-2 type cytokines inhibit NO production. For these reasons cell-mediated immunity may influence NO synthesis and mechanisms leading to iron accumulation in the RE systems (Bertero and Caligaris Cappio, 1997).

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